Faculty Opinions recommendation of Impaired antibody response causes persistence of prototypic T cell-contained virus.

2009 ◽  
Author(s):  
Marcia Blackman
Keyword(s):  
T Cell ◽  
Antibody Response

Requirement for accessory cells in the antibody response to T cell-independent antigensin vitro

1976 ◽  
Vol 6 (1) ◽  
pp. 63-68 ◽  
Author(s):  
K.-C. Lee ◽  
C. Shiozawa ◽  
A. Shaw ◽  
E. Diener
Keyword(s):  
T Cell ◽  
Antibody Response ◽  
Accessory Cells

scholarly journals Properties of the antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. IV. Special subregion assignment of the gene(s) that codes for the suppressive T-cell factor in the H-2 histocompatibility complex.

1976 ◽  
Vol 144 (3) ◽  
pp. 713-725 ◽  
Author(s):  
T Tada ◽  
M Taniguchi ◽  
C S David
Keyword(s):  
T Cell ◽  
B Cells ◽  
Antibody Response ◽  
Gene Products ◽  
T Cell Factor ◽  
Recombinant Strains ◽  
Histocompatibility Complex ◽  
Effective Suppression ◽  
Absorption Studies ◽  
Lines Of Evidence

The locus of the gene that codes for the antigen-specific suppressive T-cell factor was determined to be in a new subregion "I-J" which locates between I-B and I-C subregions in the H-2 histocompatibility complex. This was shown by two different lines of evidence: (a) The absorbing capacity for the suppressive T-cell factor of several alloantisera against restricted I subregions did not correlate with their specificity for previously known Ia molecules which are coded for by genes in I-A and I-C subregions, but was associated with the specificity for the products of genes putatively present between I-B and I-C subregions. By the occurrence of special recombinant strains, i.e. B10.A(5R), B10.A(3R), B10.S(9R), and B10.HTT, which differ with respect to the I-J subregion, we were able to produce alloantisera which distinguish I-J subregion gene products. The absorption studies using these special alloantisera directed to I-J subregion clearly indicated that the suppressive T-cell factor is a product of I-J subregion gene(s), and that the molecule is distinct from known Ia molecules expressed on splenic B cells. (b) Taking advantage of the fact that there is a strict histocompatibility requirement for the effective suppression between the donor and recipient strains of the suppressive T-cell factor, we were able to determine the required identities of the genes in the H-2 complex existing among those present between I-B and I-C. Again, utilizing the T-cell factors obtained from special recombinant strains, i.e. B10.A(4R) and B10.A(5R), we were able to locate the gene that codes for the suppressive T-cell factor reactive only with relevant haplotype strains between I-B and I-C subregions. These results are most reasonably explained by the presence of a new subregion I-J which is specialized in coding for the suppressive T-cell factor as a different molecule from previously known Ia molecules.

T Cell-Dependent Suppression of an Anti-Hapten Antibody Response

1975 ◽  
Vol 26 (1) ◽  
pp. 130-169 ◽  
Author(s):  
A. Basten ◽  
J. F. A. P. Miller ◽  
P. Johnson
Keyword(s):  
T Cell ◽  
Antibody Response

Interference with Fc signals increases an antibody response by T-cell-deprived cultures to a T-dependent antigen

1987 ◽  
Vol 107 (2) ◽  
pp. 465-470 ◽  
Author(s):  
Nicholas R.StC. Sinclair ◽  
Angela Panoskaltsis
Keyword(s):  
T Cell ◽  
Antibody Response

scholarly journals Comparison of the T Cell-Independent Antibody Response of Mice and Rats Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

1996 ◽  
Vol 32 (2) ◽  
pp. 293-297
Author(s):  
RALPH J. SMIALOWICZ ◽  
WANDA C. WILLIAMS ◽  
MARIE M. RIDDLE
Keyword(s):  
T Cell ◽  
Antibody Response ◽  
Tetrachlorodibenzo P Dioxin

scholarly journals In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations

Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3602-3608 ◽  
Author(s):  
Lee R. Silverman ◽  
Andrew J. Phipps ◽  
Andy Montgomery ◽  
Soledad Fernandez ◽  
Tomonori Tsukahara ◽  
...  
Keyword(s):  
T Cell ◽  
Antibody Response ◽  
Virus Type ◽  
Antibody Responses ◽  
Envelope Gene ◽  
Cell Leukemia Virus Type ◽  
Surface Unit ◽  
Human T Cell

AbstractHuman T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell lymphoma/leukemia (ATL). The HTLV-1 envelope gene exhibits limited variability when examined from infected individuals, but has not been tested using infectious clones of the virus in animal models. In vitro assays indicate that HTLV-1 envelope (Env) Ser75Ile, Asn95Asp, and Asn195Asp surface unit (SU) mutants are able to replicate in and immortalize lymphocytes. Herein, we examined the effects of these Env mutants in rabbits inoculated with HTLV-1 immortalized ACH.75, ACH.95, or ACH.195 cell lines (expressing full-length molecular clones with the SU mutations) or the ACH.1 cell line (expressing wild-type SU). All rabbits became infected, and the fidelity of the mutations was maintained throughout the 8-week study. However, SU point mutations resulted in decreased antibody responses to viral group-associated antigen (Gag) and Env antigens. ACH.195 rabbits had a selective decreased antibody response to SU, and one ACH.195 rabbit had an antibody response to both HTLV-1 and HTLV-2 SUs. Some mutant inoculation groups had altered proviral loads. However, peripheral-blood mononuclear cell (PBMC) proviral loads did not correlate with antibody responses. Our data are the first to demonstrate that mutations in critical determinants of HTLV-1 Env SU altered antibody responses and proviral loads, but do not prevent viral replication in vivo.

Marginal Zone B Cells Mediate a CD4 T Cell Dependent Extrafollicular Antibody Response Following RBC Transfusion in Mice

Blood ◽  
2021 ◽  
Author(s):  
Patricia E Zerra ◽  
Seema R Patel ◽  
Ryan Philip Jajosky ◽  
Connie M Arthur ◽  
James W McCoy ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Antibody Response ◽  
B Cell ◽  
T Cell Activation ◽  
Antibody Formation ◽  
Marginal Zone ◽  
Cd4 T Cell ◽  
Marginal Zone B Cells ◽  
Rbc Transfusion

Red blood cell (RBC) transfusions can result in alloimmunization toward RBC alloantigens that can increase the probability of complications following subsequent transfusion. An improved understanding of the immune mechanisms that underlie RBC alloimmunization is critical if future strategies capable of preventing or even reducing this process are to be realized. Using the HOD (hen egg lysozyme and ovalbumin fused to human Duffy) model system, we aimed to identify initiating immune factors that may govern early anti-HOD alloantibody formation. Our findings demonstrate that HOD RBCs continuously localize to the marginal sinus following transfusion, where they co-localize with marginal zone (MZ) B cells. Depletion of MZ B cells inhibited IgM and IgG anti-HOD antibody formation, while CD4 T cell depletion only prevented IgG anti-HOD antibody development. HOD-specific CD4 T cells displayed similar proliferation and activation following transfusion of HOD RBCs into wild type or MZ B cell deficient recipients, suggesting that IgG formation is not dependent on MZ B cell-mediated CD4 T cell activation. Moreover, depletion of follicular B cells failed to substantially impact the anti-HOD antibody response and no increase in antigen specific germinal center B cells was detected following HOD RBC transfusion, suggesting that antibody formation is not dependent on the splenic follicle. Despite this, anti-HOD antibodies persisted for several months following HOD RBC transfusion. Overall, these data suggest MZ B cells can initiate and then contribute to RBC alloantibody formation, highlighting a unique immune pathway that can be engaged following RBC transfusion.

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